anatomy - eo2 conceptseo2.com/resources/a_pofskin2011-02-03.pdf ·...

Copyrighted 2011 Confidential and Proprietary Information. Do Not Copy or Redistribute Without Written Permission From Electrochemical Oxygen Concepts, Inc. 12500 Network Blvd. Suite 310 San Antonio, Texas 78249 (210) 338-7300

ANATOMYAND

PHYSIOLOGYOF

WOUND HEALING


Objec7ves

Describe Key Components of Skin Anatomy and PhysiologyUnderstand the Main Func7ons of the Skin to Promote HomeostasisRecognize Differences Between Acute and Chronic Wound healingUnderstand the Phases of Wound HealingDescribe Normal and Normal Scar TissueRecognize Various Types of Wound Closure

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A & P Review of the Skin

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www.nlm.nih.gov/medlineplus/ency/imagepages/8912.htm

The short version: The skin is the largest organ on the body, it makes up about 1/6th of total body weight. It is a major part of the passive immune system and it acts as a protective wrap to keep harmful environmental agents out (micro-organisms) and allows our interaction with the world. The functions of our skin are four-fold: Protection, Sensation, Thermoregulation and Metabolic functions (Vitamin D is synthesized in the epidermis and subcutaneous fat is a major energy store). The skin is the bodys largest organ. About six pounds of skin cover eighteen square feet on an average adult. The top layer of skin is called the epidermis. It protects the underlying skin layers from the outside environment and contains cells that make kera7n, a substance that waterproofs and strengthens the skin. The epidermis also has cells that contain melanin, the dark pigment that gives skin its color. Other cells in the epidermis allow us to feel the sensa7on of touch and provide the body with immunity against foreign invaders like germs and bacteria. The very bo_om layer of the skin is the hypodermis. It contains the fat cells, or adipose 7ssue, that insulate the body and help it conserve heat. The layer between the epidermis and the hypodermis is the dermis. It contains the cells that give skin strength, support, and flexibility. As a person ages, the cells in the dermis lose their strength and flexibility, causing the skin to lose its youthful appearance. Located in the dermis are sensory receptors. They allow the body to receive s7mula7on from the outside environment and experience pressure, pain, and temperature. Small blood vessels provide the skin with nutrients, and remove its waste products. Sebaceous glands produce the oil in the skin, which keeps it from drying out. The oil from the sebaceous glands also helps to soaen hair and kill bacteria that get in the skins pores. These oil glands are all over the body, except on the palms of the hands and the soles of the feet.


Skin

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Copyrighted 2011 Confidential and Proprietary Information. Do Not Copy or Redistribute Without Written Permission From Electrochemical Oxygen Concepts, Inc. 12500 Network Blvd. Suite 310 San Antonio, Texas 78249 (210) 338-7300 5

Layers of the Skin

Lucidum

Granulosum

Spinosum

Basal

Epidermis Five Layers of cells Superficial to deep

Func7onal componentsMade up of tough, fla_ened cells of the protein kera7nCells provide barrier to injury , contaminants, light, retain water Kara7nocyts secrete protein kara7nMelanocytes produce melanin (pigment)Basal and prickle cells regenerate epidermis, produce Vit DLangerhans cells are a component of the immune system


Epidermis: Stratum Germani7vum

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Stratum Germini7vum is a single cell layerProvides germinal cells necessary for the regenera7on of the epidermisContains melanocytes which are responsible for the pigment of the skin.


Epidermis

The epidermis has an irregular shape, resembling downward fingerlike projec7ons called rete ridges or rete pegs

The significance of this anatomical structure is that the dermis has upward projec7ons The upward and downward projec7ons fit together, very much like a waffle ironThe protuberances connect, anchoring the epidermis to the dermisThis bond also helps to prevent the epidermis from sliding back and forth across the dermis with normal movement and skin manipula7on

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In healthy young skin the two layers of skin move as one. This is not the case in elderly skin over the age of 60.


Layers of the Skin

Dermal-epidermal ridges begin to fla_enTypically in the sixth decade Increased poten7al for epidermis to detach from the dermis

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As the skin ages the rete ridges begin to fla_en between the dermal- epidermal junc7on.Such epidermal/dermal fla_ening typical appears by the sixth decade of life.With this anchoring now diminished, there is an increase poten7al for the epidermis to detach from the dermis, leading to tearing of the uppermost layers of the skin, especially in the older adult popula7on- which leads to skin tears bruising ecchymosis and an increased suscep7bility to damage from pressure, fric7on and shear. From Advances in kin and wound care Vol 20(6) June 2007 pp 315-321. Preven7ng and trea7ng skin Tears Fleck, Cynthia A. MBA, BSN, RN, ET/WOCN,CWS, DNC, DAPWCA, FCCWS


Func7ons of the Skin

Protec7on fromFluid and electrolyte lossMechanical injuryUltraviolet injury

Fluid and electrolyte balance Metabolic SynthesisSensa7on/touchCommunica7onCosmesis

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***


Aging Skin

Decrease Dermal thickness Fa_y layers Collagen and elas7n fibers Size of rete ridges Sensa7on and metabolism Subcutaneous 7ssue Sweat glands

Increase Time for epidermal regenera7on Damage to skin from sun

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Gerontological Changes

With these changes Oxygen-carbon dioxide exchange decreasesTissue turnover slowsIncrease occurrence of ecchymosisInflammatory response decreasesTissue regenera7on is slower

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Threats to Skin Integrity

Pressure, fric7on, shear Moisture

Malnutri7on, dehydra7on

ImmobilityCogni7on impairments

Medica7ons (topical and systemic)

Comorbidi7es Exogenous,

endogenous and iatrogenic factors

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***


Why Do Wounds Happen?

TraumaScalds and burns physical and chemical

Animal or insects bites

Pressure

Vascular compromise,

arterial, venous or ImmunodeficiencyMalignancyConnec7ve 7ssue

disorders

Metabolic disease including diabetes

Nutri7onal deficiencies

Psychosocial disorders

Adverse effects of medica7ons

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Skin Assessment

Thorough skin assessment is paramountPreven7on is key

Address all no7fiable risk factorsEarly interven7on

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Acute vs Chronic Wound Healing

Acute or normal wound healing allows for repair of skin func7on and integrity in a 7mely manner, las7ng from 7-10 days to 2-3 weeksChronic wound healing is a disrup7on of the normal healing pathway due to underlying disease processes, infec7on, medica7ons, and varying causes that may last months to years

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Acute Wound Healing

Acute woundsInjury that occurs to the integumentInjury triggers a series of cascade/events to ini7ate hemostasis and protec7on of internal organsIn a healthy, uncompromised individual, acute wounds close/resurface spontaneously without complica7ons through the phases of wound healing=can be 2-3 weeks

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Chronic Wound Healing

Chronic WoundsWhen the phases of wound healing are delayed a chronic wound resultsLazarus, 1992 fail to progress through a normal orderly and 7mely sequence of repair or wounds that pass through the repair process without restoring anatomic and func7onal resultsClinically, wounds that do not heal within 6 weeks

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Acute & Chronic Wound Differences

Acute Wounds Low necro7c burden Low bacterial burden

Chronic Wounds High necro7c burden High bacterial burden

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*MMPs are a family of protein degrading enzymes


Hemostasis

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BMJ. 2006 April 22; 332(7547): 962965.doi: 10.1136/bmj.332.7547.962.


Hemostasis

Ini7al injury wound fills with bloodHemostasis acts by stopping hemorrhage at the wound site, decreasing blood loss, and beginning clot forma7on by way of plateletsA fine balance between cloung and bleeding is necessary to maintain wound environment

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Haemostasis is secured by platelet aggrega7on and clot forma7on. The inflammatory phase begins with the arrival of phagocy7c neutrophils and, later, macrophages at the wound site; they are important sources of and substrates for growth factors. The prolifera7ve phase is characterised by the forma7on of new blood vessels (angiogenesis), synthesis of extracellular matrix components such as collagen, granula7on 7ssue forma7on, and re-epithelializa7on. The extracellular matrix is con7nually remodeled during the final phase; an avascular scar is the end result of the healing process. Once the source of damage to a house has been removed and before work can start, u7lity workers must come in and cap damaged gas or water lines. So too in wound healing damaged blood vessels must be sealed. In wound healing the platelet is the cell which acts as the u8lity worker sealing off the damaged blood vessels. The blood vessels themselves constrict in response to injury but this spasm ul8mately relaxes. The platelets secrete vasoconstric8ve substances to aid in this Figure 1Figure 2Figure 3process but their prime role is to form a stable clot sealing the damaged vessel. Under the influence of ADP (adenosine diphosphate) leaking from damaged 8ssues the platelets aggregate and adhere to the exposed collagen3. They also secrete factors which interact with and s8mulate the intrinsic cloKng cascade through the produc8on of thrombin, which in turn ini8ates the forma8on of fibrin from fibrinogen. The fibrin mesh strengthens the platelet aggregate into a stable hemosta8c plug. Finally platelets also secrete cytokines such as platelet-derived growth factor (PDGF), which is recognized as one of the first factors secreted in ini8a8ng subsequent steps. Hemostasis occurs within minutes of the ini8al injury unless there are underlying cloKng disorders.


Prolifera7ve Phase

Epidermal cells begin to migrate across the wound bedFibroblast prolifera7on occurs and collagen is laid down forming the wound matrixForma7on of capillary buds and loops in the collagen matrix yield granula7on 7ssueThis leads to resurfacing of the defect which lasts from 4-14 days

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Platelets

Platelet aggrega7onAc7vates factor XII (Hageman) and clot forma7on beginsPlatelets release growth factors such as PDGF, TGF-alpha and TGF-beta

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Growth Factors

PDGF s7mulates neutraphils, macrophages and fibroblasts, inducing cell migra7on, prolifera7on and angiogenesisTGF-alpha is closely related to epidermal growth factor and controls epithelial cell prolifera7on and migra7onTGF-beta plays a role in cell differen7a7on, immune func7on and regulates wound matura7on and strength

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Fibrin Clot

Fibrin clot is the founda7on for the next stage of wound healingThe matrix allows for the migra7on of other cells into the wounded area to begin the inflammatory processTo avoid extended cloung, fibrinolysis occurs as well to allow con7nued migra7on of the cells

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Inflammatory Phase

Occurs within first 72 hours aaer injuryNeutrophils, mast cells and macrophages begin to migrate into the site of injuryCapillaries dilate and allow fluid into the site These lead to the typical signs of inflamma7on: redness, swelling, pain and warmth

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Mast Cells

Mast cells release histamine and serotonin which a_ract the neutraphils and macrophages to the injured areaHeparin is also released and is an an7coagulant that maintains hemosta7c balance Histamine also causes venous permeability leading to the redness and edema noted during the inflammatory process

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Neutraphils

One of the most abundant lymphocytes making up approximately 60% of the total white blood cell countOne of the first cells to arrive and they reach their highest number in the first 24-48 hoursResponsible for killing bacteria and removing debris from the wound bed, thus aiding in controlling infec7on

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Macrophages

Macrophages differen7ate from monocytes (blood) and arrive in the wound within 24-72 hoursEssen7al for wound healing as they mediate all ac7vi7es during this phase The macrophage excretes collagenases, fibronec7n (fibroblasts) and kara7nocytes which aid in debridement followed by collagen synthesis

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Lymphocytes

T-lymphocytes (thymus derived) play a significant role as the defense cells media7ng many mechanisms of the immune system responding to infected or malignant cells

There are three types of T lymphocytes: killer, helper and suppressor

B-Lymphocytes are white blood cells that originate from the bone marrow and are ac7vated by T-lymphocytes, secre7ng an7bodies to inac7vate an7gens in the bloodstream; memory cells

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Fibroblasts/Myofibroblasts

Fibroblasts produce collagen and proteoglycansNecrosis, foreign bodies and bacteria delay the development of fibroblasts and capillariesMyofibroblasts differen7ate from fibroblasts and bind 7ghtly to each other, as well as to the wound edge, causing contrac7on

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Epithelial/Endothelial

Mito7c ac7vity starts within 24-72 hours and the cells begin migra7ng across the wound bedThese cells require a smooth moist environment to migrate across the wound surfaceIf a crater or recess occurs the 7ssue may stop migra7ng or roll and form a closed wound edge called epiboly

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Matura7on Phase

Begins day 7 and can last up to 2 yearsFibroblasts leave the wound and collagen con7nues to remodel and becomes more organizedResults in a scar that is basically avascular and its tensile strength is now about 80% of the original 7ssue

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Types of Wound Closure

Primary Inten7onDelayed Primary ClosureSecondary Inten7on

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Primary Inten7on

Drawing the wound edges together to achieve closure (i.e.., surgical wounds)

Wound closure usually occurs in 3-7 daysSutures, staples, surgical glues, zippers

Decreases the risk of infec7on and allows for be_er scarring/cosmesis

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Secondary Inten7on

Wound is lea open due to infec7on or large 7ssue loss and closes by contrac7onWound edges are drawn together by contrac7le forces of the myofibroblasts ac7ng at the wound edgeWound closure can take weeks to months

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Delayed Primary Closure

To relieve 7ssue tension and to establish free drainage May be necessary due to infec7on to decrease the risk of abscess or dehiscence To prepare a wound bed for skin graaing

Allows wound to fill in large defect with granula7on 7ssue; graas require base of granula7on 7ssue for successful closure

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Skin Graas

Types include:Par7al or split thicknessFull thickness

Sources include:AutograasAllograaXenograa

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Flaps

Skin flapFree flapMuscle flapMusculocutaneous flap

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Par7al-Thickness Skin Loss

Involves destruc7on of the epidermis and can extend into but not through the dermisIt is superficial and is usually an abrasion, blister or shallow craterRegenera7on of 7ssue is full and usually without scarring

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Full-Thickness Skin Loss

Involves loss of all layers of the skin with necrosisExtensive damage to underlying structures such as muscle, tendon and bonePresents as a deep crater which may include tunneling and underminingWill never remodel back to original 7ssues due significant 7ssue loss and results in significant scarring

Dermis cannot regenerate

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Summary

The physiology of wound healing is influenced by endogenous and exogenous factorsWound closure can be facilitated by external means through proper product u7liza7on and/or surgical correc7onUnderstanding the anatomy and physiology of the skin will enhance your understanding of proper treatment op7ons

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After all, the world is full of amazing discoveries

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